In attempting to understand the various cellular events involved in the pathogenesis of EAE we have used the phenomenon of enhanced transfer to study mechanisms of immunity and inflammation in delayed-type hypersensitivity. A. Immunity: 1) Strain specificity of EAE induction in Strain 2 and Strain 13 guinea pigs; 2) Soluble factors capable of activating cells for enhanced transfer; 3) Suppression of EAE. B. Inflammation: The role played by non-specific inflammatory cells in development of EAE. C. Chronic EAE: A study of the antigens and mechanisms responsible for demyelination in the CNS. This phase of disease follows lesion initiation by antigen-specific cells and lesion development by inflammatory cells.